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Percutaneous radiofrequency ablation of hepatocellular carcinoma in the presence of portal vein thrombosis.

Portal vein thrombosis (PVT) may not be an absolute contraindication for hepatic radiofrequency ablation (RFA). Although the data are sparse, PVT is commonly considered a contraindication to RFA. PVT has actually been described as a complication following RFA. RFA was used to treat a 3.9 x 2.9 cm primary hepatocellular carcinoma (HCC) in a patient with concomitant PVT without complication. RFA can be safely performed in this setting but further studies could clarify this issue.

Carcinoma, Hepatocellular↗

Mesocaval stenting for therapy of portal hypertension after orthotopic liver transplantation.

A 20-year-old patient underwent liver transplantation (LT) because of chronic hepatitis-associated cirrhosis. After transplantation, the patient developed partial portal vein thrombosis without deterioration of liver function. However, in the long-term follow-up, the patient developed refractory portal hypertension with recurrent episodes of severe upper gastrointestinal bleeding. Extensive nonoperative treatment including multiple esophageal ligatures and sclerotherapy was not successful. Thus, the patient had to be treated surgically with a mesocaval H-shunt. Pathophysiology, therapy and prognosis of this rare complication after LT are discussed with regard to the literature.

Adult↗

[Hepatic encephalopathy after injection of lanreotide, a somatostatin analog].

We report one case of hepatic encephalopathy following the administration of a somatostatin analogue (lanreotide) in a patient with a pancreatic endocrine tumor and liver metastases. Hepatic insufficiency was absent. The diagnosis of hepatic encephalopathy relied upon a positive re-challenge test, elevated veinous ammonemia, suggestive findings on electroencephalogram and lack of recurrence after lanreotide discontinuation. Encephalopathy was thought to be due to a significant decrease in hepatic blood flow caused by lanreotide; an associated thrombosis of the portal vein may have played a facilitating role.

Aged↗

Variceal hemorrhage: efficacy of transjugular intrahepatic portosystemic shunts created with Strecker stents.

PURPOSE: To evaluate the efficacy of transjugular intrahepatic portosystemic shunts (TIPS) in treatment of variceal hemorrhage. MATERIALS AND METHODS: Forty-five patients with cirrhosis underwent TIPS placement for treatment of acute (n = 12) or recurrent (n = 33) variceal hemorrhage. Shunts were created with Strecker stents. RESULTS: Shunts were established by deployment of stents in 42 patients. The portosystemic pressure gradient decreased from an average of 20.4 mm Hg +/- 5.4 to 9.2 mm Hg +/- 4.1. Complications included hepatic failure (n = 1), acute shunt thrombosis (n = 2), right jugular vein thrombosis (n = 1), bacteremia (n = 1), and stent misplacement (n = 1). Acute bleeding was controlled in 12 patients. The 30-day mortality rate was 2%; four other patients have since died. During follow-up (mean, 8.9 months), variceal bleeding recurred in six patients. Hepatic encephalopathy developed in six patients. Shunt stenosis or occlusion requiring further intervention occurred in 20 patients. CONCLUSION: TIPS are safe and effective in treatment of variceal hemorrhage; however, secondary interventions are often required to preserve shunt function.

Constriction, Pathologic↗

Incidence, risk factors, management, and outcome of portal vein abnormalities at orthotopic liver transplantation.

Portal vein thrombosis is often considered a contraindication to orthotopic liver transplantation. We have analyzed the incidence, risk factors, management and outcome of patients with portal vein thrombosis undergoing orthotopic liver transplantation. During the period from October 1988 to October 1992 140 grafts were performed on 132 patients. Fourteen had portal vein thrombosis with either partial (n = 7) or complete (n = 7) occlusion of the portal vein at surgery. Portal vein thrombosis was more common in patients with autoimmune chronic active hepatitis (3/5 vs. 11/127, chi 2 = 13.3, P < 0.001), cryptogenic cirrhosis (4/12 vs. 10/120, chi 2 = 7.2, P < 0.01), or those with tumors (6/22 vs. 10/110, chi 2 = 5.7, P < 0.05). In 13 of the 14 portal inflow was reestablished by flushing, balloon thrombectomy, or passage of a graduated dilator. In one patient complete fibrous obliteration necessitated a portal vein to right gastroepiploic vein anastomosis. On follow-up there have been 6 deaths in this group (6/14 = 43%) from recurrent cancer (n = 1), sepsis (n = 4), and cardiac and renal failure (n = 1). Four of these 6 patients had confirmation of PV patency on imaging. The remaining 8 patients are alive and well (median follow-up 37 months, range 6-53 months). Post-transplant portal vein thrombosis occurred in 3 of the 14 patients (21%) with a portal vein abnormality at surgery and in two of the 118 patients with a normal portal vein (3/14 vs. 2/118, chi 2 = 8.5, P < 0.01). Four of the 5 cases were successfully treated by surgical thrombectomy.

Adolescent↗

Anemic necrosis of the liver after umbilical vein catheterization.

We report 22 cases of hepatic necrosis following catheterization of the umbilical vein. The morphology of the necrotic lesions, which were confined to the left lobe in 21 patients, was that of an anemic infarct. Their causes are multiple and include intimal damage during the insertion of the catheter with consecutive thrombosis of portal vein branches, the postpartum immaturity of the arterial hepatic oxygen supply, postpartum hypoxia due to respiratory failure of cerebral or pulmonary origin, obstruction of portal venous flow through the catheter as such, the postpartum involution of the left hepatic lobe, and prolonged periods of catheterization. Toxic damage of the hepatic parenchyma due to an infusion of Tris buffer through the catheter into the portal venous system is a potential additional factor.

Catheterization↗

Persistence of embryonic pattern of hepatocaval venous junction and patent ductus venosus in Budd-Chiari syndrome.

We report an autopsy study on a case of Budd-Chiari syndrome (BCS) in a 44-year-old woman. Dissection showed that the outlets of the right hepatic vein (HV) and of the common trunk of the middle and left HVs appeared as two small depressed areas with narrow ostia. Histological examination showed recent thrombosis of the tributaries of the HVs and centrilobular congestion with necrosis of the hepatic parenchyma. The juxtacaval portions of the major HVs showed a cuneiform shape, because of marked dilation, with thread-like ostia, and multiple small outlets of minor hepatic veins were also present. The coexistence of patent ductus venosus may have prevented the development of the hepatocaval venous junction, with persistence of the embryonic pattern, composed of multiple small channels draining into the right hepatocardiac channel. The unusual hepatocaval venous junction may have predisposed to thrombosis of the HVs, causing BCS.

Adult↗

Advances in pediatric liver transplantation: continuous monitoring of portal venous and hepatic artery flow with an implantable Doppler probe.

BACKGROUND: Acute vascular thrombosis is a dreaded complication in solid organ transplantation. Pediatric liver transplantation is associated with a high incidence of hepatic artery thrombosis. Graft salvage is dependent upon early recognition and correction of the thrombosis. Current methods of surveillance for vascular thrombosis lack early detection. METHODS: Four consecutive pediatric liver transplantations were performed using the implantable Doppler probe to monitor the patency of the hepatic artery and the portal vein during the early postoperative period. RESULTS: The implantable Doppler probes provided reliable monitoring of vascular patency. Early detection of hepatic artery thrombosis, with subsequent correction and graft salvage, was achieved with the use of the implantable Doppler probe. CONCLUSIONS: The implantable Doppler probe provides real-time surveillance of vascular patency for up to 7 days in the postoperative period. Signal quality and character was easily assessed by physician and nursing staff and reliably reflected intravascular flow.

Adolescent↗

Endovascular treatment of obliterative hepatocavopathy with inferior vena cava occlusion and renal vein thrombosis.

We describe the endovascular treatment of an occlusion of the inferior vena cava (IVC) due to obliterative hepatocavopathy with renal and iliac vein thrombosis. A 34-year-old man with nephrotic syndrome and hepatic dysfunction presented to the hospital after a 3-month history of lower extremity swelling with an acute deterioration in his condition. Magnetic resonance venography diagnosed a massive IVC occlusion with thrombosis of the entire IVC, iliac veins, and renal vein. He was treated with thrombolysis, and a chronic occlusion of the infrahepatic IVC was discovered. After venous stenting of the IVC and iliac veins, he dramatically improved. After 24 months, he remains symptom-free with a patent IVC and iliac veins.

Adult↗

Surgery for hilar cholangiocarcinoma; a 10 year experience of a tertiary referral centre in the UK.

OBJECTIVE: To review the outcome of patients operated for hilar cholangiocarcinoma and analyse prognostic variables. PATIENTS AND METHODS: A prospectively collected database on patients with hilar cholangiocarcinoma, between 1992 and 2003, and relevant clinical notes were reviewed retrospectively. A total of 174 patients, 96 male, median age 63 years (27-86), were referred. Jaundice was the initial presentation in 167. RESULTS: ERCP was the initial interventional investigation at the referring centre in 150, of which only 30 were stented successfully. PTC and decompression was carried out on 120. In 17, combined PTC and ERCP were required for placement of stents. Seventy-two underwent laparotomy at which 27 had locally advanced disease. Forty-five had potentially curative resections. Extra hepatic bile duct resection was done in 14 patients of which four were R0 resections. Thirty-one had bile duct resection including partial hepatectomy with 19 R0 resections (P=0.042). Post-operative complications developed in 19 patients, and there were 4 30 day mortalities [hepatic insufficiency:/sepsis (n=3), thrombosis of the reconstructed portal vein (n=1)]. Among the patients with R0 resections, the cumulative survival rates at 1, 3, and 5 year; was 83, 58, 41%, respectively, and in those with R1 resections were 71, 24, 24%, respectively, (P=0.021). Overall survival was shorter in patients with positive perineural invasion (P=0.066: NS). There was no significant difference in survival between the node positive and negative group. Median survival of patients who underwent liver resection was longer than those with bile duct resection only (30 vs 24 months P=0.43: NS). CONCLUSIONS: ERCP was associated with a high failure rate in achieving pre-operative biliary decompression which was subsequently achieved by PTC. Clear histological margins were associated with improved survival and were better achieved by liver resection as compared to extra hepatic bile duct resection. Positive level I lymph nodes did not adversely impact survival.

Adenocarcinoma↗

Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia.

A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels.

Femur Head Necrosis↗

[Pathogenesis and surgical tactics in the extrahepatic form of portal hypertension in children].

The correlation analysis of different parameters of the oxygen regimen of the liver, its blood circulation and angioarchitectonics were used in 44 patients in order to reveal different ways of the compensation of blood flow depending on the form of blockade (in thrombosis of the portal vein--at the expense of the hepatic artery, in its malformation--at the expense of the formation of porto-portal collaterals). The operation of choice is thought to be gastrotomy with ligation of varicose veins of the stomach and esophagus from the side of mucosa. It was used in 110 patients and in 88% of the cases recurrent bleedings were prevented for the period up to 15-20 years.

Adolescent↗

Transjugular intrahepatic portosystemic shunt for the treatment of portal hypertension secondary to non-cirrhotic perisinusoidal hepatic fibrosis.

Non-cirrhotic perisinusoidal hepatic fibrosis is a process of imprecise pathogenesis involving collagenization of the space of Disse. Exposure to chemicals, auto-immunity, thrombophilia and/or infections are suspected primary agents. Here, we present the case of a patient who developed severe portal hypertension with histological features suggesting a non-cirrhotic perisinusoidal hepatic fibrosis. A 52-year-old man was hospitalized for oesophageal variceal haemorrhage. Liver cirrhosis or portal vein thrombosis were absent as attested by laboratory tests, duplex sonography, computed tomography scan and histological examination of a liver biopsy specimen. Presinusoidal portal hypertension was suggested by a normal wedge-free hepatic vein gradient. Only electron microscopy examination of a liver biopsy specimen could disclose perisinusoidal fibrosis. This was most probably secondary to a combined chemotherapy received 4 years earlier for non-Hodgkin large-cell lymphoma. As variceal ligation failed to control oesophageal varices while liver function tests were normal, a transjugular intrahepatic portosystemic shunt (TIPS) was performed. This dramatically improved the signs of portal hypertension. This case illustrates the use of TIPS in the treatment of portal hypertension secondary to non-cirrhotic perisinusoidal fibrosis.

Esophageal and Gastric Varices↗

[Successful treatment of postoperative multiple hepatic recurrence with hepatic arterial infusion of cisplatin and degrable starch microspheres].

A 38-year-old man had multiple recurrence of hepatocellular carcinoma (HCC) with portal vein thrombosis after hepatectomy and postoperative transcatheter arterial chemotherapy with 5-fluorouracil (5-FU). He was treated by trans hepatic arterial embolization (TAE) with 100 mg of cisplatin (CDDP) and degrable starch microspheres (DSM). After 3 courses were administered, the recurrent lesions almost disappeared on CT, and the postoperative rise in PIVKA-II level and AFP level normalized. There were no side effects except slight fever and general fatigue. We recognized a partial response, and the patient is still alive 14 months after hepatectomy. This case suggests that TAE with CDDP and DSM might be useful for prolonging the survival of advanced HCC patients.

Adult↗

[Massive venous thrombosis with cardiac invasion as primary manifestation of hepatocarcinoma].

Hepatocellular carcinoma has a tendency to invade vascular structures. However, extension into the hepatic veins or heart is uncommon. We describe the case of a 68 years old man with chronic viral hepatitis type C, consulting about edema and pain in his left leg. Doppler scan showed deep venous thrombosis in that level and computed tomography of thorax and abdomen showed complete thrombosis of the inferior cava vein, thrombosis of the left suprahepatic vein, a voluminous thrombus in the right atrium and an irregular mass in the liver. Alpha-fetoprotein was 77,046 ng/ml The biopsy of the rigth atrium thrombus demonstrated diseminated hepatocellular carcinoma. We comment the patient progress after surgery, the incidence, clinical symptoms, and therapy options for these patients.

Aged↗

Natural history of compensated viral B and D cirrhosis.

AIM: The aim of this study was to define the natural long-term course of HDV compensated cirrhosis. METHODS: 166 consecutive patients with compensated HDV-related cirrhosis diagnosed since 1994 were followed up until the first decompensation and then until death, liver transplantation or 31st of December 2004. The survival during follow-up and the survival according to the type of first decompensation were calculated using the Kaplan Meier method. Survival curves were compared using the log-rank test. RESULTS: 56 females (33.7%) and 110 males (66.3%) with a mean age of 40.7+/-7.9 years were included in the study. The mean Child Pugh and MELD score at the first episode of hepatic decompensation was 8.6+/-2.08 and 15.19+/-5.42, respectively. The median survival was 58.3 months since the diagnosis of compensated cirrhosis and the mean time to first decompensation was 21+/-19 months. The probability of survival after the diagnosis of compensated cirrhosis was 94.3%, 82.5%, and 51.5% at 1, 2, and 5 years, respectively. Ascites was the most frequent first decompensation (80.7%), followed by jaundice (30.1%), portal hypertensive gastrointestinal bleeding (PHGIB) (28.9%), hepatic encephalopathy (HE) (12%), hepatocellular carcinoma (HCC) (12%), portal vein thrombosis (8.4%), spontaneous bacterial peritonitis (SBP), hepatorenal syndrome. 86 patients (51.8%) presented more than one complication at initial decompensation. Survival was worse in patients with jaundice and SBP (p=0.001), followed by patients with HE (p=0.05) and patients who presented more than one initial complication (p=0.03). In the multivariate survival analysis only PHGIB as first decompensation and MELD score>15 were independent predictors of death. CONCLUSION: HDV-related cirrhosis in Romania is an aggressive disease with a median time to decompensation less than 2 years and a median survival less than 5 years. Jaundice, the main clinical consequences of portal hypertension and HCC are the most frequent causes of decompensation and more than half the patients present two or more concomitant initial complications.

Adolescent↗

[Imaging of complications of liver transplantation in children].

The authors report their experience of imaging of 286 liver transplantations (LT) in children. Hepatic artery thrombosis is the most serious complication (9%), with a maximum risk during the first two weeks. Its clinical presentation is very variable and its diagnosis is based on Doppler ultrasonography. Emergency surgical disobstruction prevented the development of biliary or ischaemic complications in one half of cases. Portal thrombosis (4.5%) is due, in the majority of cases, to hypoplasia of the recipient's portal vein. Patency of intrahepatic portal branches with inversion of flow can delay the ultrasonographic diagnosis. Biliary complications are frequent (20%) and occur after a very variable interval. Their diagnosis is ultrasonographic, but sometimes delayed compared to the histological signs. Transhepatic cholangiography visualises the lesions and allows external drainage or even percutaneous dilatation. In 1 out of 4 cases, the aetiology was hepatic artery thrombosis. The imaging protocol after LT consists of ultrasonography with daily Doppler (or even twice-daily) in the patient's bed for the first two weeks and then as required. Computed tomography is useful to demonstrate parenchymal ischaemia and intraperitoneal abscess in multi-operated children. Angiography and cholangiography confirm the ultrasonographic signs. Interventional Radiology plays an increasingly important role.

Aortography↗

Autoimmune complications associated with hepatitis A virus infection in children.

Hepatitis A virus infection is usually a self-limited disease during childhood. Autoimmune manifestations are rarely reported among patients. We describe two children with acute hepatitis A infection who developed immune thrombocytopenia and hepatic venous thrombosis during the course of acute infection. Antiphospholipid antibodies were increased in both of them during the thrombocytopenic and thrombotic complications and decreased during the resolution of these events.

Acute Disease↗